In hemochromatosis the monocyte-macrophage appears to be deficient in the ability to store iron. This flaw may represent a relative incapacity to synthesize ferritin. (Crosby, New Engl. J. Med. 296: 1116, 1977). The distinctive flaw in patients with hemochromatosis is the inability of the small intestine to refrain from absorbing available iron that the body does not need. Because of no excretory mechanism for iron, the unneeded iron is placed in storage to the ultimate detriment of the storage tissues. These two flaws may be related. The monocyte-macrophage may be the agent whereby the intestine is informed (in hemochromatosis misinformed) concerning the body's iron requirement. We propose several lines of investigation of the monocytes' participation in iron metabolism. 1. Synthesis of ferritin in vitro by normal human monocytes and monocytes of patients with hemochromatosis. 2. Movement of iron-loaded macrophages through the blood and through tissues. 3. The effect of chronic alcoholic intoxication in rats on the movement of iron-loaded macrophages. 4. EM studies of cell-cell behavior between macrophages and epithelial cells of the iron-absorptive intestinal mucosa. 5. Transplantation of marrow from humans with hemochromatosis into lethally irradiated mice to learn if such a chimera is unable to control the absorption of irons.